AJP - Cell Physiology, Vol 269, Issue 3 C766-C774, Copyright © 1995 by American Physiological Society

ARTICLES

ATP depletion inhibits capacitative Ca2+ entry in rat thymic lymphocytes

I. Marriott and M. J. Mason
Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana 70112, USA.

The present study investigates the requirement for cellular ATP in the increase in plasma membrane Ca2+ permeability activated by the release of Ca2+ from intracellular stores in rat thymic lymphocytes (capacitative Ca2+ entry). The permeability state of this pathway following activation with thapsigargin was probed in control and ATP-depleted cells using fluorometric measurements of intracellular Ca2+, Mn2+ entry, and membrane potential, and unidirectional measurements of Ca2+ uptake using 45Ca2+. The capacitative Ca(2+)-entry pathway was markedly inhibited in cells depleted of ATP by incubation in glucose-free solution containing oligomycin, antimycin A, and 2-deoxy-D-glucose. These data cannot be explained on the basis of a loss of the transmembrane electrochemical gradient for Ca2+, alterations in intracellular pH or cellular Na+ content, a direct effect of the inhibitors of ATP production on the capacitative Ca(2+)-entry pathway, or the ability of thapsigargin to release Ca2+ from intracellular stores. Rather, these data are consistent with a requirement for ATP or a high-energy phosphate donor in the activation and/or maintained activation of capacitative Ca2+ entry.

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